title: [Effect of electroacupuncture on thymocyte apoptosis-related genes in morphine withdrawal rats].
abstract: OBJECTIVE
  To explore the underlying mechanism of electroacupuncture (EA) in relieving morphine withdrawal syndrome in rats.
  
  
  METHODS
  Forty SD rats were randomly divided into normal control group, model group 1, model group 2 and EA group. Morphine withdrawal syndrome model was established by muscular injection of morphine (5 mg/kg on the 1st day, progressively increasing everyday till 100 mg/kg on the 20th day) in the hind limbs. Then, rats of model group 1 were anesthetized (10% chloraldurat) to be killed on the 21st day, and those of model group 2 killed on the 27th day. EA (2/100 Hz, 2-4 mA) was applied to bilateral "Zusanli" (ST 36) for 30 mm, once a day for 7 days. The rat's thymus was removed (after anesthesia), cut into sections (4 pm) and stained with immunohistochemical method for displaying the expression of apoptotic promoters Bax, Fas, Fas Ligand (FasL) as well as anti-apoptotic peptide Bcl-2.
  
  
  RESULTS
  Compared with normal group, Bcl-2 immunoreaction (IR)-positive cell number of model group 1 and group 2 decreased significantly while Sax, Fas and FasLIR-positive cell number and Bax/Bcl-2 in two model groups increased considerably (P < 0.01). In comparison with model group 2, Bcl-2 IR-positive cell number of model group 1 decreased significantly (P < 0.05), Bax, Fas and FasL IR-positive cell number and Bax/Bcl-2 of model group 1 were significantly higher (P < 0.01, fl. 05). After EA, in comparison with model group 2, Fas and FasL IR-positive cell number and Bax/Bcl-2 decreased significantly (P < 0.01, 0.05), and Bcl-2 IR-positive cell number increased markedly in EA group (P < 0.05); in comparison with model group 1, Bcl-2 IR-positive cell number increased significantly (P < 0.01), while Bax, Fas and FasL IR-positive cell number and Bax/Bcl-2 decreased evidently in EA group (P < 0.01).
  
  
  CONCLUSIONS
  EA at "Zusanli" (ST 36) can inhibit morphine-induced downregulation of Bcl-2 and upregulation of Fas and FasL expression, which may contribute to its effect in resisting thymus apoptosis in morphine withdrawal rats.
authors.affiliation: Institute of Acu-moxibustion, An-hui College of Chinese Medicine, Hefei 230038, China. zsongxg0128@163.com
authors.forename: Xiao-ge
authors.initials: XG
authors.lastname: Song
authors.forename: Yong-lei
authors.initials: YL
authors.lastname: Zhu
authors.forename: Rong-jun
authors.initials: RJ
authors.lastname: Zhang
authors.forename: Yao
authors.initials: Y
authors.lastname: Zhang
authors.forename: Xian-hua
authors.initials: XH
authors.lastname: Liu
mesh_terms: D000818:Animals; D051017:Apoptosis Regulatory Proteins / Q000235:genetics / Q000378:metabolism*; D015671:Electroacupuncture; D053222:Fas Ligand Protein / Q000235:genetics / Q000378:metabolism*; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D008297:Male; D009020:Morphine / Q000378:metabolism*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013375:Substance Withdrawal Syndrome / Q000628:therapy*; D013950:Thymus Gland / Q000166:cytology / Q000378:metabolism; D019014:fas Receptor / Q000235:genetics / Q000378:metabolism*
chemical_list: D051017:Apoptosis Regulatory Proteins; D053222:Fas Ligand Protein; D019014:fas Receptor; D009020:Morphine